Evidence map›Paper›PMID 34593902›Full record

ArticleScientific reports2021

Suppression of autophagy promotes fibroblast activation in p53-deficient colorectal cancer cells.

Takanori Inoue, Yoshito Hayashi, Yoshiki Tsujii, Shunsuke Yoshii, Akihiko Sakatani, Keiichi Kimura, Ryotaro Uema, Minoru Kato, Hirotsugu Saiki, Shinichiro Shinzaki and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Genetic variants in autophagy-related geneFrontiers in oncology · 2022
    Article
  7. Review
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Takanori InoueDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Yoshito HayashiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Yoshiki TsujiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Shunsuke YoshiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Akihiko SakataniDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Keiichi KimuraDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Ryotaro UemaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Minoru KatoDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Hirotsugu SaikiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Shinichiro ShinzakiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Hideki IijimaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan. takehara@gh.med.osaka-u.ac.jp.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficiency of p53 in cancer cells activates the transformation of normal tissue fibroblasts into carcinoma-associated fibroblasts; this promotes tumor progression through a variety of mechanisms in the tumor microenvironment. The role of autophagy in carcinoma-associated fibroblasts in tumor progression has not been elucidated. We aimed to clarify the significance of autophagy in fibroblasts, focusing on the TP53 status in co-cultured human colorectal cancer cell lines (TP53-wild-type colon cancer, HCT116; TP53-mutant colon cancer, HT29; fibroblast, CCD-18Co) in vitro. Autophagy in fibroblasts was significantly suppressed in association with ACTA2, CXCL12, TGFβ1, VEGFA, FGF2, and PDGFRA mRNA levels, when co-cultured with p53-deficient HCT116

Indexed as

AutophagyAutophagy-Related ProteinsBiomarkers, TumorCancer-Associated FibroblastsCell Line, TumorCells, CulturedCoculture TechniquesColorectal NeoplasmsExosomesGene Expression Regulation, NeoplasticHCT116 CellsHumansMicroRNAsModels, BiologicalTumor MicroenvironmentTumor Suppressor Protein p53ATG2B protein, humanAutophagy-Related ProteinsBiomarkers, TumorMicroRNAsTP53 protein, humanTumor Suppressor Protein p53Vesicular Transport Proteins

Identifiers

PMID34593902
PMCPMC8484348
OpenAlexW3125976025

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.